Hall J E, Guyton A C
Am J Physiol. 1976 Nov;231(5 Pt. 1):1550-6. doi: 10.1152/ajplegacy.1976.231.5.1550.
The effect of increased plasma oncotic pressure on renal blood flow (RBF), glomerular filtration rate (GFR), electrolyte excretion, and renin secretion rate (RSR) was studied in dogs anesthetized with sodium pentobarbital. Renal artery infusions of hyperoncotic dextran or human serum albumin raised renal venous colloid osmotic pressure an average of 7.3 and 10.1 mmHg, respectively, and caused small but consistent increases in RBF, large increases in RSR, marked decreases in urine flow rate and electrolyte excretion, with either no change or small decreases in GFR, and no change in renal artery pressure. Renal vasodilation was confined primarily to afferent arterioles and was not measureable until approximately 45 s after the start of infusions. The renal responses to increased plasma oncotic pressure appeared to be an autoregulatory phenomenon, consistent with a tubular mechanism dependent on an altered distal tubular fluid flow and/or composition. The increased renin release during increased plasma oncotic pressure is not compatible with a renal baroreceptor mechanism that responds to decreases in afferent arteriolar pressure because calculated glomerular pressure increased during albumin and dextran infusions.
在戊巴比妥钠麻醉的犬身上,研究了血浆胶体渗透压升高对肾血流量(RBF)、肾小球滤过率(GFR)、电解质排泄和肾素分泌率(RSR)的影响。经肾动脉输注高渗右旋糖酐或人血清白蛋白,分别使肾静脉胶体渗透压平均升高7.3和10.1 mmHg,并使RBF出现小幅度但持续的增加,RSR大幅增加,尿流率和电解质排泄显著减少,GFR无变化或略有下降,肾动脉压力无变化。肾血管舒张主要局限于入球小动脉,且在输注开始约45秒后才可测量到。肾脏对血浆胶体渗透压升高的反应似乎是一种自身调节现象,符合一种依赖于远端肾小管液流量和/或成分改变的肾小管机制。血浆胶体渗透压升高期间肾素释放增加,这与肾压力感受器机制不相符,因为在输注白蛋白和右旋糖酐期间,计算得出的肾小球压力升高,而该机制是对入球小动脉压力降低做出反应的。